Effect of B on Microstructure and Properties of Surfacing Layer of Austenitic Stainless Steel Flux Cored Wire.

In order to study the effect of element B on the corrosion resistance of stainless steel-based flux cored wire surfacing alloy, a stainless steel surfacing layer was prepared on the surface of carbon steel plate by melt electrode gas shielded welding, and then the microstructure, electrochemical corrosion resistance, and wear resistance of the surfacing layer were analyzed. The results show that the surfacing layer of surfacing alloy presents M2B and Fe3(C, B) phases based on austenite. Boride formed in deposited metal has good corrosion resistance. Therefore, adding the proper amount of B can significantly improve the corrosion resistance of the surfacing layer. When the boron content is 2%, the corrosion resistance is the best. The minimum self-corrosion current density is 1.75766 × 10-11 mA·cm2, and the maximum self-corrosion potential is -0.254438 V. Maximum impedance curve radius. At this time, the wear resistance of the surfacing layer is also the best.

Managing Emergent Surgery for Ruptured Abdominal Aortic Aneurysm during the COVID-19 Pandemic.

BACKGROUND: Coronavirus disease 2019 (COVID-19) has become a global pandemic which may compromise the management of vascular emergencies. An uncompromised treatment for ruptured abdominal aortic aneurysm (rAAA) during such a health crisis represents a challenge. This study aimed to demonstrate the treatment outcomes of rAAA and the perioperative prevention of cross-infection under the COVID-19 pandemic. METHODS: In cases of rAAA during the pandemic, a perioperative workflow was applied to expedite coronavirus testing and avoid pre-operative delay, combined with a strategy for preventing cross-infection. Data of rAAA treated in 11 vascular centers between January-March 2020 collected retrospectively were compared to the corresponding period in 2018 and 2019. RESULTS: Eight, 12, and 14 rAAA patients were treated in 11 centers in January-March 2018, 2019, and 2020, respectively. An increased portion were treated at local hospitals with a comparable outcome compared with large centers in Guangzhou. With EVAR-first strategy, 85.7% patients with rAAA in 2020 underwent endovascular repair, similar to that in 2018 and 2019. The surgical outcomes during the pandemic were not inferior to that in 2018 and 2019. The average length of ICU stay was 1.8 ± 3.4 days in 2020, tending to be shorter than that in 2018 and 2019, whereas the length of hospital stay was similar among 3 years. The in-hospital mortality of 2018, 2019, and 2020 was 37.5%, 25.0%, and 14.3%, respectively. Three patients undergoing emergent surgeries were suspected of COVID-19, though turned out to be negative after surgery. CONCLUSIONS: Our experience for emergency management of rAAA and infection prevention for healthcare providers is effective in optimizing emergent surgical outcomes during the COVID-19 pandemic.

I-BET726 suppresses human skin squamous cell carcinoma cell growth in vitro and in vivo.

Bromodomain-containing protein 4 (BRD4) is a potential therapeutic target of skin squamous cell carcinoma (SCC). I-BET726 is a novel BRD4 inhibitor. Its potential effect in skin SCC cells was tested in the present study. We show that I-BET726 potently inhibited survival, proliferation, cell cycle progression, and migration in established (A431/SCC-9/SCC-12/SCC-13 lines) and primary human skin SCC cells. I-BET726 induced significant apoptosis activation in skin SCC cells. It was more efficient in inhibiting skin SCC cells than known BRD4 inhibitors (JQ1, CPI203, and AZD5153). I-BET726 not only downregulated BRD4-regulated proteins (c-Myc, Bcl-2, and cyclin D1), but also inhibited sphingosine kinase 1 (SphK1) and Akt signalings in SCC cells. Restoring Akt activation, by a constitutively active S473D mutant Akt1 ("caAkt1"), partially inhibited I-BET726-induced cytotoxicity in A431 cells. In vivo, I-BET726 oral administration potently inhibited A431 xenograft growth in severe combined immunodeficient mice. Downregulation of BRD4-regulated proteins and inhibition of the SphK1-Akt signaling were detected in I-BET726-treated A431 xenograft tumor tissues. Together, I-BET726 inhibits skin SCC cell growth in vitro and in vivo.

Study on Improvement of Welding Technology and Toughening Mechanism of Zr on Weld Metal of Q960 Steel.

Q960 high-strength steel is widely used in pressure vessels, bridges, offshore platforms and other important steel structural components because of its high strength and good plastic toughness, but alloy elements added to this kind of steel have strong hardenability, especially after welding, so the strength and toughness cannot meet the requirements, which limits its application in a wider range. In this paper, from the point of view of the metallurgical treatment of the weld, the goal is to improve the strength and toughness of the Q960 high strength steel weld metal In order to analyze the influence of Zr on the welding process of Q960 steel and the strengthening and toughening effect of weld metal, this paper takes Fe-Mn-Mo-Cr-Ni as the main alloy system, BaF2-CaF2-Al-Mg as the basic slag system, and adopts the method of melting consumable electrode self-shielded for welding, and analyzes the welding process, microstructure, tensile property and impact toughness of the welded joint. The experimental results show that when the weld metal contains 0.0061% Zr, the minimum spatter rate is only 7%, the maximum slag removal rate is 95%, the maximum hardness is 357HV, the maximum elongation is 34%, and the impact toughness is the highest. At this time, the acicular ferrite content in the weld microstructure is the highest, and there is a certain amount of equiaxed fine-grained ferrite, and the content of proeutectoid ferrite is the least, which effectively improves the strength and toughness of the weld metal.

Baseline and early 3D-CUBE volume reconstruction of locally advanced rectal cancer to predict tumor response after neoadjuvant chemotherapy.

PURPOSE: To explore whether volumetric measurements of 3D-CUBE sequences based on baseline and early treatment time can predict neoadjuvent chemotherapy (NCT) efficacy of locally advanced rectal cancer (LARC). MATERIAL AND METHOD: 73 patients with LARC were enrolled from February 2014 to January 2018. All patients underwent MRIs during the baseline period before NCT (BL-NCT) and the first month of NCT (FM-NCT), and tumor volume (TV) was measured using 3D-CUBE, and tumor volume reduction (TVR) and tumor volume reduction rate (TVRR) were calculated. In addition, tumor invasion depth, tumor maximal length, range of tumor involvement in the circumference of intestinal lumen and distance from inferior part of tumor to the anal verge were measured using baseline high-spatial-resolution T2-weighted MRIs. All patients were categorized into sensitive and insensitive groups based on post-surgical pathology after completion of the full courses of NCT. The receiver operating characteristic (ROC) curve was used to analyze the value of different MRI parameters in predicting efficacy of NCT. RESULTS: Statistically significant differences in TV of BL-NCT, TVR and TVRR from BL-NCT to FM-NCT were detected between sensitive and insensitive groups (P < 0.05, respectively). The areas under the curves (AUC) of ROC of TVR and TVRR in predicting efficacy of NCT (0.890 [95% CI, 0.795∼0.951], 0.839 [95% CI, 0.735∼0.915]) were significantly better than that of TV (0.660 [95% CI, 0.540∼0.767]) (P < 0.05, respectively). CONCLUSION: Reconstruction of 3D-CUBE volume in the first month of NCT is necessary, and both TVR and TVRR can be used as early predictors of NCT efficacy.

Urinary Metabolomics to Identify a Unique Biomarker Panel for Detecting Colorectal Cancer: A Multicenter Study.

BACKGROUND: Population-based screening programs are credited with earlier colorectal cancer diagnoses and treatment initiation, which reduce mortality rates and improve patient health outcomes. However, recommended screening methods are unsatisfactory as they are invasive, are resource intensive, suffer from low uptake, or have poor diagnostic performance. Our goal was to identify a urine metabolomic-based biomarker panel for the detection of colorectal cancer that has the potential for global population-based screening. METHODS: Prospective urine samples were collected from study participants. Based upon colonoscopy and histopathology results, 342 participants (colorectal cancer, 171; healthy controls, 171) from two study sites (Canada, United States) were included in the analyses. Targeted liquid chromatography-mass spectrometry (LC-MS) was performed to quantify 140 highly valuable metabolites in each urine sample. Potential biomarkers for colorectal cancer were identified by comparing the metabolomic profiles from colorectal cancer versus controls. Multiple models were constructed leading to a good separation of colorectal cancer from controls. RESULTS: A panel of 17 metabolites was identified as possible biomarkers for colorectal cancer. Using only two of the selected metabolites, namely diacetylspermine and kynurenine, a predictor for detecting colorectal cancer was developed with an AUC of 0.864, a specificity of 80.0%, and a sensitivity of 80.0%. CONCLUSIONS: We present a potentially "universal" metabolomic biomarker panel for colorectal cancer independent of cohort clinical features based on a North American population. Further research is needed to confirm the utility of the profile in a prospective, population-based colorectal cancer screening trial. IMPACT: A urinary metabolomic biomarker panel was identified for colorectal cancer with the potential of clinical application.

Publisher Correction: NOS1 S-nitrosylates PTEN and inhibits autophagy in nasopharyngeal carcinoma cells.

It was brought to the attention of the Editors that there had been an accidental duplication of the western blot images during the preparation of Figs. 1b and c. The authors were notified about the error and have supplied the correct image for Fig. 1c (below). We apologize for any inconvenience this may have caused readers.

Portopulmonary Hypertension: A Complex Case Derived from Multiple Penetrating Trauma-Induced Mesenteric Arteriovenous Fistulae.

Portopulmonary hypertension (PoPH) is a well-recognized complication of portal hypertension. This study reports a case of PoPH that was secondarily caused by post-traumatic mesenteric arteriovenous fistula. A 38-year-old man with a history of knife stabbing wounds in the abdomen in 2003 was admitted to the hospital with exertional shortness of breath and a mechanic murmur over the umbilical region. Computed tomography indicated signs of PoPH and mesenteric arteriovenous fistula. Percutaneous catheter-directed embolization was first performed but failed. Subsequently, the patient was successfully treated with fistula resection and partial enterectomy. The patient had been postoperatively followed regularly, and chief symptoms had been alleviated significantly and pulmonary pressure had successfully decreased to normal range. We believe that this is the first case of PoPH caused by mesenteric arteriovenous fistula.

IGF2BP1 over-expression in skin squamous cell carcinoma cells is essential for cell growth.

The present study examined expression and potential functions of insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in human skin squamous cell carcinoma (SCC). We show that IGF2BP1 mRNA and protein expression levels were upregulated in established (A431 line) and primary human skin SCC cells. Its expression was also increased in human skin SCC tissues, as compared to the normal skin tissues. In skin SCC cells, IGF2BP1 silencing or CRISPR/Cas9 knockout decreased levels of IGF2BP1-stablized mRNAs, including IGF2, CD44, Gli1 and Myc. Furthermore, skin SCC cell survival and proliferation were inhibited by IGF2BP1 silencing/knockout. Conversely, forced over-expression of IGF2BP1 further promoted A431 cell survival and proliferation. Furthermore, siRNA-mediated knockdown of IGF2BP1-bound long non-coding RNA THOR ("Lnc-THOR") similarly depleted IGF2BP1-dependent mRNAs, causing inhibition on A431 cell survival and proliferation. In vivo, IGF2BP1 silencing or knockout inhibited A431 tumor xenograft growth in mice. Together, we conclude that IGF2BP1 over-expression in skin SCC cells is essential for cell growth.

Features and treatment of gas-forming synergistic necrotizing cellulitis: a nine-year retrospective study.

BACKGROUND: As many doctors know little about gas-forming synergistic necrotizing cellulitis, we retrospectively explored it in our study. METHODS: Totally, 30 patients diagnosed with gas-forming synergistic necrotizing cellulitis between November 2006 and September 2015 were included. They were divided into two groups: open drainage group (19 patients) and aggressive debridement group (11 patients). Retrospectively analyzed data comprised demographic characteristics, APACHE II scores, pathogen culture results, bleeding amount during the operation, white blood cell count, length of hospital stay and recovery. RESULTS: The mortality rate was 26% in the open drainage group and 73% in the aggressive debridement group (p=0.023). There was no statistical difference in the APACHE II score before treatment between the open drainageand aggressive debridement groups (16.6±4.5 vs 18.1±7.5, p=0.511). The APACHE II score was significantly higher after treatment in the aggressive debridement group (14.2±5.8 score vs 20.1±9.1, p=0.038). There were no statistical differences in the white blood count cell before and after treatment (13.49 × 109±5.05×109 cells/L vs 17.46×109±6.94×109 cells/L, p=0.082; 10.37×109±3.54×109 cells/L vs 15.47×109 ±7.51×109 cells/L, p=0.055; respectively). The bleeding amount during the operation was significantly more in the aggressive debridement group (315±112 ml vs 105±45 ml, p<0.001. CONCLUSION: For treating gas-forming synergistic necrotizing cellulitis, performing open drainage as early as possible isthe most important procedure after admission.

Hairy/enhancer of Split Homologue-1 Suppresses Vascular Endothelial Growth Factor-induced Angiogenesis via Downregulation of Osteopontin Expression.

Angiogenesis plays a critical role in the progression and vulnerability of atherosclerotic plaques; however, the orchestration of angiogenesis in atherosclerotic plaque formation remains unclear. The results of microarray analysis, real-time PCR and immunohistochemical analyses showed that Hairy/enhancer of split homologue-1 (Hes-1) expression was significantly decreased, while that of osteopontin (OPN) was increased, in atherosclerotic plaques. Meanwhile, immunofluorescence results demonstrated that both Hes-1 and OPN were expressed in endothelial cells (ECs) of neovessels in atherosclerotic plaques. The results of an in vitro study showed that Hes-1 was downregulated, while OPN was upregulated, in a time- and dose-dependent manner in human umbilical vein endothelial cells (HUVECs) by VEGF treatment. In addition, Hes-1 knockdown was found to have transcriptional promotion effect on OPN expression in HUVECs and enhance OPN-induced angiogenesis in response to VEGF. On the contrary, Hes-1 overexpression inhibited OPN expression in HUVECs and reduced angiogenesis in vitro and in vivo. The results of this study suggest that decreased Hes-1 expression in atherosclerotic plaques exaggerate VEGF-induced angiogenesis by upregulating OPN. Therefore, restoring Hes-1 expression and inhibiting OPN expression may be a promising strategy to prevent vulnerable plaque formation in patients with atherosclerosis.

iNOS-derived nitric oxide promotes glycolysis by inducing pyruvate kinase M2 nuclear translocation in ovarian cancer.

Aerobic glycolysis is essential for tumor growth and survival. Activation of multiple carcinogenic signals contributes to metabolism reprogramming during malignant transformation of cancer. Recently nitric oxide has been noted to promote glycolysis but the mechanism remains elusive. We report here the dual role of nitric oxide in glycolysis: low/physiological nitric oxide (≤ 100 nM) promotes glycolysis for ATP production, oxidative defense and cell proliferation of ovary cancer cells, whereas excess nitric oxide (≥ 500 nM) inhibits it. Nitric oxide has a positive effect on glycolysis by inducing PKM2 nuclear translocation in an EGFR/ERK2 signaling-dependent manner. Moreover, iNOS induced by mild inflammatory stimulation increased glycolysis and cell proliferation by producing low doses of nitric oxide, while hyper inflammation induced iNOS inhibited it by producing excess nitric oxide. Finally, iNOS expression is abnormally increased in ovarian cancer tissues and is correlated with PKM2 expression. Overexpression of iNOS is associated with aggressive phenotype and poor survival outcome in ovarian cancer patients. Our study indicated that iNOS/NO play a dual role of in tumor glycolysis and progression, and established a bridge between iNOS/NO signaling pathway and EGFR/ERK2/PKM2 signaling pathway, suggesting that interfering glycolysis by targeting the iNOS/NO/PKM2 axis may be a valuable new therapeutic approach of treating ovarian cancer.

NOS1 S-nitrosylates PTEN and inhibits autophagy in nasopharyngeal carcinoma cells.

Autophagy is a cellular survival mechanism that involves the catabolic degradation of damaged proteins and organelles during periods of metabolic stress, and when overly stimulated, commonly contributes to cell death. Nitric oxide (NO), a potent cellular messenger, participates in a complex mechanism which assists in controlling autophagy. However, the mechanism by which endogenous NO formed by distinct isoforms of nitric oxide synthase (NOS) helps to regulate autophagy in cancer cells remains unclear. Here we report that NOS1 reduces excessive levels of autophagy and promotes the survival of nasopharyngeal carcinoma cells. We found that inhibition of NOS1 increased cell death resulting from siRNA or the use of pharmacologic agents; and this effect was reversed by the autophagy inhibitor, chloroquine. The role of NOS1 in the autophagy process depended on the activation of AKT/mTOR signaling by S-nitrosylation of phosphatase and tensin homolog (PTEN) proteins. The mechanism by which NOS1 modifies PTEN protein might involve a direct interaction between these two molecules. Moreover, in an in vivo study, the NOS1 inhibitor N(G)-nitro-L-arginine methyl ester activated AKT/mTOR signaling and promoted autophagy in xenograph tumors. Our studies demonstrated that NOS1 prevents excessive autophagy via S-nitrosylation of PTEN, and activation of the AKT/mTOR signaling pathway. PTEN and the AKT/mTOR signaling pathway are promising targets for improving the chemotherapeutic treatment of cancer.

WISP1 overexpression promotes proliferation and migration of human vascular smooth muscle cells via AKT signaling pathway.

Proliferation and migration of vascular smooth muscle cells (VSMCs) play crucial roles in the development of vascular restenosis. Our previous study showed that CCN4, namely Wnt1 inducible signaling pathway protein 1 (WISP1), significantly promotes proliferation and migration of rat VSMCs, but its mechanism remains unclear. This study aims to investigate whether and how WISP1 stimulates proliferation and migration of human VSMCs. Western blot analysis showed that FBS treatment increased WISP1 protein levels in human VSMCs in a dose-dependent manner. Overexpression of WISP1 using adenovirus encoding WISP1 (AD-WISP1) significantly increased proliferation rate of human VSMCs by 2.98-fold compared with empty virus (EV)-transfected cells, shown by EdU incorporation assay. Additionally, Scratch-induced wound healing assay revealed that adenovirus-mediated overexpression of WISP1 significantly increased cell migration compared with EV-transfected cells from 6h (4.56±1.14% vs. 11.23±2.25%, P<0.05) to 48h (25.25±5.51% vs. 97.54±13.12%, P<0.01) after injury. Transwell Migration Assay confirmed that WISP1 overexpression significantly promoted human VSMC migration by 2.25-fold compared with EV. Furthermore, WISP1 overexpression stimulated Akt signaling activation in human VSMCs. Blockage of Akt signaling by Akt inhibitor AZD5363 or PI3K inhibitor LY294002, led to an inhibitory effect of WISP1-induced proliferation and migration in human VSMCs. Moreover, we found that WISP1 overexpression stimulated GSK3α/ß phosphorylation, and increased expression of cyclin D1 and MMP9 in human VSMCs, and this effect was abolished by AZD5363. Collectively, we demonstrated that Akt signaling pathway mediates WISP1-induced migration and proliferation of human VSMCs, suggesting that WISP1 may act as a novel potential therapeutic target for vascular restenosis.

Recurrent inflammatory myofibroblastic tumor of the inguinal region: A case report and review of the literature.

Inflammatory myofibroblastic tumors (IMTs) of the inguinal region are exceptionally rare. The current study reported the case of a 49 year-old male patient with IMT, who presented with a fever, night sweats, anorexia, loss of weight and frequent urination. Computed tomography (CT) revealed a lesion occupying the soft tissue of the right inguinal region and surgery was performed to resect the lesion. Histopathological analysis of the lesion revealed a composition of spindle and inflammatory cells, including plasma cells and lymphocytes. In addition, immunohistochemical analysis demonstrated that the tumor cells were positive for CD34, vimentin, actin, Ki-67, B cell lymphoma-2, CD99, epithelial membrane antigen and CD38; however, tumor cells were negative for CD117, desmin, anaplastic lymphoma kinase and creatine kinase. Thus, the patient was diagnosed with IMT and was advised to return for regular follow-up appointments. Subsequently, the patient developed a local recurrence 12 months following the initial surgery. Of note, the histopathological characteristics of the recurrent lesions were consistent with those of the initial specimen. Thus, a second surgery was performed, followed by fractionated radiotherapy (FRT). At 3 and 6 months following the FRT, magnetic resonance imaging scans did not indicate tumor recurrence or metastasis. In conclusion, surgical excision is the current recommended treatment for IMT; however, for cases similar to that of the current study, which are not successfully controlled by surgical excision, radiotherapy should be considered and long-term follow-up is essential.

Diagnostic efficacy of whole-body diffusion-weighted imaging in the detection of tumour recurrence and metastasis by comparison with 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography or computed tomography in patients with gastrointestinal cancer.

OBJECTIVE: The primary aim of this study was to assess the efficacy of whole-body diffusion-weighted imaging (WB-DWI) in detecting tumour recurrence and metastasis of gastrointestinal cancers by comparison with 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography or computed tomography ((18)F-FDG-PET/CT). A secondary aim was to evaluate the change of apparent diffusion coefficient (ADC) value between metastases and normal tissues. METHODS: Twenty-eight previously confirmed gastrointestinal cancer patients with suspected tumour recurrence or metastasis were recruited. WB-DWI and PET/CT images were evaluated by two radiologists and a nuclear medicine physician. Agreement between WB-DWI and PET/CT for detective efficacy was compared using kappa statistics. Additionally, diagnostic accuracy, sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) were also statistically analysed. ADC values between metastatic and normal tissues were compared. RESULTS: There was no statistically significant difference (P > 0.05) in the overall diagnostic performances of PET/CT (accuracy 98.9%; sensitivity 95.2%; specificity 99.8%; PPV 98.9%; NPV 98.9%) and WB-DWI (accuracy 95.9%; sensitivity 81.7%; specificity 99.1%; PPV 95.0%; NPV 96.1%). WB-DWI showed agreement with PET/CT (κ = 0.877) for detecting recurrence and distant metastases. A statistically significant difference in ADC value was observed between tissues of normal healthy volunteers and metastases in lymph nodes, liver and bones (P < 0.05). CONCLUSIONS: WB-DWI is reliable in detecting tumour recurrence and metastasis of colorectal cancer and offers the same diagnostic performance as (18)F-PET/CT without ionizing radiation. The quantitative value of ADC provides extra information to determine cancer metastasis.

An unusual presentation of type II Abernethy malformation.

Abernethy malformation is a rare anomaly of the splanchnic venous system. We report a case of an unusual portosystemic shunt via a dilated inferior mesenteric vein. A 20-year-old woman was referred to our hospital with complains of nonspecific abdominal pain for almost 3 years and hematochezia since 15 months old. Computed tomography and further transhepatic splenoportography revealed a hypoplastic portal vein and a giant inferior mesenteric vein, via which part of the portal venous blood drained into the inferior vena cava. The patient underwent a surgical ligation of the portocaval shunt and recovered well. We believe that this is the first case of type II Abernethy malformation presenting as a portosystemic shunt via the giant inferior mesenteric vein.

CCN4 regulates vascular smooth muscle cell migration and proliferation.

The migration and proliferation of vascular smooth muscle cells (VSMCs) are essential elements during the development of atherosclerosis and restenosis. An increasing number of studies have reported that extracellular matrix (ECM) proteins, including the CCN protein family, play a significant role in VSMC migration and proliferation. CCN4 is a member of the CCN protein family, which controls cell development and survival in multiple systems of the body. Here, we sought to determine whether CCN4 is involved in VSMC migration and proliferation. We examined the effect of CCN4 using rat cultured VSMCs. In cultured VSMCs, CCN4 stimulated the adhesion and migration of VSMCs in a dose-dependent manner, and this effect was blocked by an antibody for integrin α5ß1. CCN4 expression was enhanced by the pro-inflammatory cytokine tumor necrosis factor α (TNF-α). Furthermore, knockdown of CCN4 by siRNA significantly inhibited the VSMC proliferation. CCN4 also could up-regulate the expression level of marker proteins of the VSMCs phenotype. Taken together, these results suggest that CCN4 is involved in the migration and proliferation of VSMCs. Inhibition of CCN4 may provide a promising strategy for the prevention of restenosis after vascular interventions.

Aluminum oxide mask fabrication by focused ion beam implantation combined with wet etching.

A novel aluminum oxide (Al2O3) hard mask fabrication process with nanoscale resolution is introduced. The Al2O3 mask can be used for various purposes, but in this work it was utilized for silicon patterning using cryogenic deep reactive ion etching (DRIE). The patterning of Al2O3 is a two-step process utilizing focused ion beam (FIB) irradiation combined with wet chemical etching. Gallium (Ga(+)) FIB maskless patterning confers wet etch selectivity between the irradiated region and the non-irradiated one on the Al2O3 layer, and mask patterns can easily be revealed by wet etching. This method is a modification of Ga(+) FIB mask patterning for the silicon etch stop, which eliminates the detrimental lattice damage and doping of the silicon substrate in critical devices. The shallow surface gallium FIB irradiated Al2O3 mask protects the underlying silicon from Ga(+) ions. The performance of the masking capacity was tested by drawing pairs consisting of a line and an empty space with varying width. The best result was seven such pairs for 1 µm. The smallest half pitch was 59 nm. This method is capable of arbitrary pattern generation. The fabrication of a freestanding single-ended tuning fork resonator utilizing the introduced masking method is demonstrated.

[Experience with endovenous laser treatment combined with high ligation and Muller's phlebectomy for C3-6 grade primary superficial varicose in the lower limbs].

OBJECTIVE: To summarize the experience with endovenous laser treatment(EVLT) combined with high ligation and Muller's phlebectomy for primary superficial varicose in the lower limbs. METHODS: In 95 patients with C3-6 grade primary superficial varicose in 146 lower limbs, the extent of varicose was accurately marked, the guiding wires were manipulated precisely, and the proximal great saphenous veins (GSV) were ligated after exsanguinations. The stems of the GSV were ablated with laser with the lower limbs lift up and pressed hard along the stems, and Muller's incisions were carefully planned. RESULTS: All the operations were completed successfully. The guiding wires entered into the deep veins through the communicating branches in 2 limbs, 1 patient experienced capillary hemorrhage from Muller's incisions, 8 had thrombotic phlebitis of the GSV, 7 sustained heat-related injury of the saphenous nerves, 1 experienced skin heat-related lesion, 2 developed hematoma in the inguinal region, 2 had pitting edema in the dorsum of the foot, 1 had fat liquefaction of the Muller incision, and 1 showed rejection of the thrum. After conservative treatment, all the patients recovered and were discharged. Part of the superficial varicose remained after the operation in 6 limbs. CONCLUSION: It is necessary to standardize the routine procedure of EVLT combined with high ligation and Muller's phlebectomy to reduce the complications.